The heart is located in the chest and is the only circulatory pump that distributes oxygenated blood to the tissue. It is a hollow muscular organ lined with three layers of branched, striated cellular muscular tissue. These muscle cells, the myocytes, are layered in sheets and have timed automaticity and contractility as specialised qualities. Intercalated discs, special for the heart, replace conventional cell membranes and join adjacent myocytes to form sheets of muscle wrapped around like a turban forming two ejectile ventricular chambers that cater to the systemic and pulmonary circulations. In addition, these discs help propagate an initiated action potential so that a ventricle can contract as a single unit.
Microscopically the contractile unit, the sarcomere, is nucleated, bounded by a sarcolemmal membrane, and contains the contractile proteins - myosin, actin, tropomyosin and troponin. The striated appearance is due to these intracellular contractile proteins' linear arrangement and partial overlapping. The syncitial and fibrillar arrangement of the heart as an organ is endowed with the following unique properties:-
Excitability,
Rhythmicity,
Conductivity,
Contractility.
These help to maintain the dynamic nature of the mammalian circulation.
Blood returns to the heart through veins into relatively passive atrial chambers. The respective atrial and ventricular septa effectively separate oxygenated and de-oxygenated blood and thus the systemic left-sided and the pulmonary right-sided circulatory pathways are created. It is interesting to note here that the whole circulatory system of humans is in a series and the contractile force of the left ventricle is enough to drive blood through rhythmically. The stimulus for contraction is a depolarisation
originating automatically in the Purkinje tissue of the sinoatrial (SA) node. The contraction starts at the apical region of a ventricle, is progressive, has a leftward twist nearing the end of contraction, and propels forward blood into the arterial tree. So for the contraction to be effective only a fraction of the myocytes needs shortening.
Heart failure is a unique situation that may be due to a variety of reasons, both intracardiac and extracardiac. In every situation, the physician strives to go to the root of the problem and manage accordingly. Extracardiac causes are commonly organ-specific and medical management suffice. In occasional cases like that of co-arctation of the aorta, with or without a PDA, aortic dissection, aorto-aortitis, hepato-renal failures, etc. surgical intervention may be necessary. Similarly, surgery is not the answer for all intracardiac patients with heart failure. An inventory of the major reasons makes it further relevant:--
Cardiomyopathies -
a) dilated --- implantation of a Cardiac Resynchronisation Device (CRT) may ease the symptoms in some, but the longevity remains the same.
b) hypertrophic -- (i)-Endomyocardial fibroelastosis --- extensive debridement of fibroelastic tissue may be done in selected cases, but results are questionable.
(ii)-Idiopathic apical septal hypertrophy --- transaortic apical septal myectomy is the classic procedure when the left ventricular outflow obstruction (LVOTO) becomes life-threatening. A less invasive transcatheter first septal artery apical septal embolisation became popular for a time but was discarded as the infarction could not be controlled.
c) ischaemic -- it can again be focal, regional, and global. The treatment in all these situations is coronary revascularisation, either the less-invasive percutaneous transcatheter angioplasty and stenting or the surgical coronary artery bypass as some degree of pathological coronary block compromises the nutrient-rich arterial flow to the heart.
Significant regional wall motion abnormalities (RWMA) lead to geometric changes in ventricular cavitary shape, and consequently, the internal wall stress increases exponentially. For such subjects, a Batista type of left ventricular infarcectomy may be helpful.
The Dor infarcectomy, apical reconstruction with repair of the VSD due to the ischemic ventricular septal rupture is reserved for managing adult ischemic VSDs.
d) infections, especially viral --- the cardiomyopathy is global and management is conservative. Only when the viability is in question and there is little recoverable myocardium, a transplant is the logical answer.
Valve-related - Both stenotic and regurgitant lesions create volume-related problems, though in a different manner. Myocardial contractility is affected in separate ways at various stages and in chronic regurgitant lesions of the mitral valve, the measured ejection fraction may increase. The pathophysiology of acute cases is different. The results are best when surgical intervention is done before the failing myocardium irreversibly loses contractile strength. However, it has to be remembered that prosthetic replacement of a diseased heart valve, be it metallic or a bioprosthesis, makes the base of the heart immobile and thus the ejection fraction is reduced as compared with the baseline for this patient.
Right ventricular dysplasia and atrialisation of the non-functional right ventricle -
Dysplasia of the right ventricle is usually focal and the reason behind the sudden trigger of life-threatening arrhythmias. Prolonged arrhythmias can cause circulatory failure.
Atrialisation of a portion of the right ventricle is a feature of Ebsein anomaly and is treated by imbrication of the atrialised portion during repair.
Pericardial diseases interfering with cardiac contractility -
In constrictive pericarditis and thickened nonresilient (fibrotic or calcific with or without some amount of fluid) pericardium, cardiac contractile ejection is severely compromised until the restrictive jacket is removed.
Any fluid within the pericardial space decreasing contractility is tamponade and urgent drainage is warranted.
Tumours and other miscellany -
Discrete cardiac space-occupying lesions (SOL) should be excised without delay, preserving as much contractile myocardium as possible. Atrial myxoma is common, but rhabdomyoma has a greater affinity for the ventricular muscles.
Case reports of cardiac hydatid cysts are not uncommon and they can be found in unusual places - the following is an example of multiple hydatid cysts of the interventricular septum (personal collection).
InfiltrativInfiltrative diseases like amyloidosis and secondary malignancies have no long-term or effective surgical cure due to progressive replacement, invasion of the myocytes, and extensive multisystem involvement.
The heart is one of the most important organs in the body. A debate about the seat of mind is still ongoing. Investigations have been numerous and the physicians' goal has always been to find out the reason, current state, stage progression, and treatability of heart failure in a non-invasive or minimally invasive way from the outside. The electrocardiogram (ECG) was the earliest to develop other than auscultation and pulse. With the advent of surgery and the understanding that the heart could withstand some manipulations, other investigations rapidly developed. A set of investigations was recommended for a suspected clinical condition and among all the various forms and modes of echocardiography (ECHO) proved most useful and informative. The echocardiogram was able to give a comprehensive idea about --
Any structural defects and septal continuity,
Contractile nature and force of the myocardium,
RWMAs and dyskinesia of any region,
Valvular function and competence,
Nature of leaflet coaptation, thickness and pliability,
Degree of valvular obstruction or leak,
Presence of SOLs, outflow and inflow obstructing lesions,
Cardiac dimensions and derived functions.
In addition, a tissue Doppler helps to get a realistic idea about the tissue's nature, and stress echo with a tolerable inotrope ascertains the ability, response, and degree of myocardial thickening in myocardial strain. As the question of shock and hibernation following an insult is still present, either a Technetium 99-m radioisotope scan or a cardiac MRI should be done to determine myocardial viability.
Heart failure symptomatology is varied and encompasses a wide range. The degree of ventricular systolic or diastolic dysfunction determines the nature of heart failure. Left ventricular (sided) systolic dysfunction is the most common type of heart failure and the symptoms include --
Shortness of breath or dyspnoea to ordinary activity usually comes on suddenly,
Easy fatiguability,
Hunger for fresh air,
Third space fluid accumulation in the remote circulatory areas like the -
a) feet, legs, and ankles,
b) small of the back,
c) lungs, especially while lying flat,
pitting oedema characterises the first two conditions, while in the third situation, a pink-frothy sputum is the hallmark.
Harassing cough,
Increased nocturnal frequency of urination,
Tachyarhythmia.
The situation can be acute or chronic and acute exacerbation of a chronic build-up is the usual scenario.
A right-sided contractile failure commonly occurs in volume-overloaded states and the complaints in most situations look like congestion due to further inflow of venous blood into the right side of the heart, The right ventricle, though more compliant, is stretched beyond the limits and fails to pump adequate amounts of blood into the pulmonary circuit. In accommodating greater amounts of blood from the already overloaded right ventricle, the latter exhibits a higher pressure - pulmonary hypertension. This pulmonary hypertension, in turn, hinders the forward propulsion of blood into the arterial tree of the lungs for oxygenation.
Conditions leading to diastolic dysfunction and failure are as follows:--
Atrial fibrillation and similar arrhythmias affecting hemodynamics,
Diabetes,
Hypertension,
Obesity,
Obstructive sleep apnoea
Improper and unbalanced dietary habits.
Undue stress and a sedentary lifestyle.
Right-sided heart failure is usually secondary to a complex congenital heart defect, a lung condition, or a major venous thrombosis and the common findings are --
weight gain,
limb swellings/puffy face,
ascites,
visible tortuous subcutaneous veins on the abdomen or chest depending upon the site of obstruction.
respiratory distress especially when lying flat.
A left ventricular failure may lead to a right ventricular diastolic dysfunction and failure. In actual practice, there may be right ventricular diastolic dysfunction, cavitary compromise and even a right ventricular failure preceding the actual left ventricular systolic failure in worsening aortic stenosis; This is a classical Bernheim phenomenon where left ventricular thickening and rightward convexity of the interventricular septum in response to the rising intraventricular pressure cause right ventricular cavity compromise and dysfunctional diastolc failure of the right ventricle. Reverse Bernheim phenomena have also been noticed when an overloaded right ventricle compromises the left ventricular cavity. Intraventricular cavitary geometry plays an important part in generating ventricular contractile force.
This situational shifting of the interventricular septum is also called ventricular interdependence.
Both the ventricles can fail together, which is called a biventricular failure. Left and right ventricular failure symptoms may present simultaneously and confuse a physician.
The term congestive heart failure is common and is a late stage where the contractile force of the ventricles is weak and at the same time, venous return to the right side of the heat is slowed to such an extent that fluid retention occurs in the third space. For the state of congestive heart failure to happen both the ventricles should fail in unison. The inability of ventricular myocardial contractility may in turn be due to systolic or diastolic dysfunction and a mix of systolic and diastolic dysfunction of the two ventricles, combined with congestive heart
The American College of Cardiology (ACC) and the American Heart Association (AHA) first
classified heart failure based on risk factors, structural changes, and the severity of symptoms. Classes A, B, C, and D were assigned accordingly. The ACC/AHA later classified heart failure based on the subject's ejection fraction. This ECHO-based classification mentions the following subdivisions:--
Heart failure with preserved ejection fraction - HFpEF.
Heart failure with reduced ejection fraction - HFrEF.
Heart failure with moderately or mildly reduced ejection fraction - HFmrEF,
Heart failure with improved ejection fraction - HFimpEF (new addition).
WHO endorses this and code-10 is earmarked by the International Classification of Diseases (ICD). The European Society of Cardiology (ESC) guidelines for heart failure (HF) provide evidence-based recommendations for diagnosis and treatment. Prevention, diagnosis, and treatment are the basic tenets of managing heart failure. The guidelines also include recommendations for:-
Implantable cardioverter-defibrillators,
Cardiac resynchronization therapy implantation,
Exercise rehabilitation,
Multidisciplinary interventions.
Again the functional class, state, and stage of heart failure is to be considered. The New York Heart Associaton proposed a clinical classification that has been universally accepted and the four NYHA classes are:
Class I
No limitations, - ordinary physical activity does not cause undue fatigue, shortness of breath, or palpitations
Class II
Slight limitations,- ordinary physical activity causes fatigue, shortness of breath, palpitations, or angina
Class III
Marked limitations, -less than ordinary physical activity causes fatigue, shortness of breath, palpitations, or angina
Class IV
Severe limitations and symptoms occur at rest, and any physical activity increases discomfort
Clinicians often use the NYHA classification system to help with risk stratification and treatment decisions. When natriuretic peptide levels and echocardiographic ejection fraction are also considered, the state of failure at that particular time becomes evident.
There is a subtle difference between the current state and the stages of heart failure, The stages of failure are interchangeable, and according to guidelines there are the following four stages:---
Stage A: At risk for heart failure | People who are at risk for heart failure but do not yet have symptoms or structural or functional heart disease Risk factors for people in this stage include hypertension, coronary vascular disease, diabetes, obesity, exposure to cardiotoxic agents, genetic variants for cardiomyopathy and family history of cardiomyopathy |
Stage B: Pre-heart failure | People without current or previous symptoms of heart failure but with either structural heart disease, increased filling pressures in the heart or other risk factors |
Stage C: Symptomatic heart failure | People with current or previous symptoms of heart failure |
Stage D: Advanced heart failure | People with heart failure symptoms that interfere with daily life functions or lead to repeated hospitalizations |
Heart failure is a complicated and critical condition. Detection commonly happens when symptoms appear and early diagnosis becomes a reality with the prior knowledge of inciting conditions, stress, and lifestyle. Diagnosis is clinical and the NYHA class, current state of the failure with measurement of natriuretic peptides, and echocardiography for evaluation of ejection fraction are necessary for corroboration. Staging of heart failure is mainly for counselling. Coronary revascularization is the most common surgery for heart failure and other surgeries are required in limited and selected situations only.
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